So it confuses a lot of students. And I'm only saying a lot of this stuff over like six times in different repetitions. It's funny how we learn this. Now before we get to that, I made some additions to your unit five material folder. I put in a sheet with blood pressure medicines and this.
You all are going to have to do some prioritization on this test. That resultation, another patient, So if you've looked through the little PDF that I gave you, there should have been a scenario. So there was a scenario in there that kind of went through. We'll talk about that one in a little bit. But yesterday I had to teach this to the main campus students and I didn't give them all of this.
This is just for you. But it's I don't want to confuse them all. But when you're prioritizing, typically we're going to start with the ABCs. Airway, breathing, circulation.
Is there an issue there? If it's non-airway breathing, circulation, is it a Maslow's? Is it physiological over social or emotional? It's not that. Is it an acute problem or a chronic problem?
If you can't just figure it out, just go through the list and think what's going to kill them first. That's probably going to be the answer. So on this, It's just for you to look at.
We're not going to go through this, but it's to help you practice prioritization. Does that sound like something you'll do? I've got to trash talk some of y'all at the main campus a little bit. Well, they've never had me down there. And they were like, well, do we need to read this chapter?
Is this chapter 14? I'm like, I gave you a very explicit reading list. with you and somebody confirmed earlier they asked if I was pulling questions from them yes it's like I go from the old Cheryl mentor days that if I don't pull questions from the readings you're not going to do them still not going to do them in some cases so yeah I kind of trashed y'all a little bit but they were for the most part not pleasant people down there more or a nicer comfortable bunch I guess not not not you but But for the most part, you guys are a lot more social. So good there. Now, the autonomic nervous system.
We have two people here. It's kind of just summarizes it in the best way that any image creator can do. That on the left, you've got somebody that looks anxious and nervous.
On the right, you've got somebody resting and eating. And that's basically how autonomic nervous system breaks down. It comes in two parts. We've got the sympathetic side, which is all about getting the body ready to run and jump and fight or get the heck out of here.
In a stressful situation, the sympathetic nervous system usually kicks in. When you were doing your test today, did you have palpitations? Did you feel stress?
Yes. So that's kind of what happens when you experience stress. Your body starts spewing out.
things like adrenaline kicks the sympathetic nervous system into effect. Me, I did not have a stressful situation to go through today. So my sympathetic nervous system was like, eh, whatever. I'm in the rest of digestion mode right now. I wish I was.
Good for you. I'm hungry. Yay me. Well, I'm going to be as soon as we get out of here, actually. Yeah.
I'll probably just go with the drop. The hard part about this is it's the autonomic nervous system because you typically don't have control over it. You can't tell your heart, okay, go 120 beats a minute. It's outside of your control. It's usually like psychological, social triggers that kick these into gear.
Is that like flight or flight? Yes. Okay. And right there is your slide.
Oh. Flight or flight. So, the gist of it is the autonomic part of your nervous system is broken down into that fight or flight, which is the sympathetic response. That something has come up and frightened you. Your body starts shooting out adrenaline.
Become more focused. It's either you're going to have to run from the tiger or fight the tiger, basically. Or tiger, lions, tigers, bears, whatever. Now the other part, the parasympathetic, it's all about when you don't have to exert a lot of energy. Your body is more focused on digesting food, recovering from whatever you were running from before.
This is St. Clairville. It's one of the sites where you're sitting in the fall. Okay.
So this is it. We have two opposing parts of the autonomic nervous system. Basically the gist of what it is.
Now, the sympathetic is going to do what? Activate in stressful situations. Parasympathetic?
Resting. Moving the food through. Your body doesn't need to prime itself for a lot of energy expenditure. So it's all about processing the stuff. There are some mnemonics that we'll talk about a little bit later, but this is just the gist of it.
They typically work kind of like that. Have you all seen the like the little scales where you can see things way equally? The old timey ones, they balance out.
This is usually how they work. They kind of work, try to keep you in a state of homeostasis. That something stressful happens, sympathetic will kick in, keep you alive. Then that's over.
We go back into that little balance state. So here's what... We're talking about when we talk about organs being innervated or parts of the body being innervated with the different parts.
The left-hand side, again, it's run, get out of here, fight. There's another F2, but we don't talk about that for the last place. We don't talk about that.
Other side, resting. Now, this just shows how organs are innervated. The sympathetic side, pubis, airways. parts of the stomach, bladder, adrenals. Those are all parts that are things that need to either be activated or held back on when you're in a stressful situation.
Bladder, let's use that as an example. So you're being chased down the yellow brick road by a line of tiger and bear on line. Okay?
They may have cats. What do cats like? If something pees on the porch or something, what are they doing?
They're all about smells. So if you are running down the aisle with your throat and the cowardly lion is not so cowardly in chasing you, is it helping you in this situation to be like peeing right down your legs? No.
So the sympathetic nervous system kind of clenches that little sphincter muscle so that you're not peeing all over the place when you're going to Your pupils, your eyes, it's going to tell your pupils to shoot open, to dilate, to let more light in so you can see better. It's going to increase your heart rate because you've got to get blood going to the tissues that need it, the muscles. The GI tract, that's not important to you.
You don't need to have explosive diarrhea while you're being chased by something. So it slows GI tract stuff down. Okay, so just think of it as...
what the body needs at that moment. Now the liver, the liver has something from the sympathetic side running into it. We haven't talked about it in any of the classes that I'm getting in. There's something stored in the liver. Your body will store glycogen.
Glycogen is basically like a big clump of sugar molecules. So it's there and puts your body needs a little So what happens is the sympathetic nervous system sends a signal there and says, "Hey, emergency happening. We need to get a little extra sugar boost going on." So it breaks down glycogen and releases glucose through your cell state. Now, the parasympathetic side, in a lot of cases, it does the opposite reaction. The pupils, you don't need all that extra light, so they'll get stripped. You're getting ready to, you're in the rest and digest phase.
So in the mouth it's going to increase salivation. It's going to increase movement through the GI tract. Peristalsis will increase. And that's what happens on each side when the receptors are activated for each division. Now the receptors are activated by a couple of things.
There's more than a couple but we're just going to get to them. In the sympathetic nervous system, You've all heard of adrenaline, right? Getting a big adrenaline rush.
So there's also noradrenaline. We call those epinephrine and norepinephrine, mostly. So those are the two big neurotransmitter triggers in the sympathetic nervous system. And they're going to activate those alpha and beta receptors, which are also part of the sympathetic nervous system.
Now, the parasympathetic runs on acetylcholine. The receptors that it activates, we're gonna talk about muscarate receptors. There is another called nicotinic receptors, but we're not talking about those.
It'll be 54 weeks until I do the lecture on the nicotinic receptors in the myasthenia gravis section. So for our purposes this semester, alpha receptors, beta receptors, muscarinic receptors. I think that's enough for you right now unless you want to go more. It's our choice.
We don't want to go more. Now dopamine is considered an adrenergic sympathetic transplant. We're not going to worry about that one.
We talk about that more when you get into some of the cardiac issues. Like we need to increase cardiac output for somebody that has certain types of shock. So even though dopamine might be listed in your textbook in some of the sections, we're not worried about it right now.
Epi and norepi. Now, looking at this, you can see that they don't always activate the same receptors. And that's important later on. Epinephrine is the master key in the sympathetic nervous system. If there's a receptor to be activated, it's going to activate it.
Now, norepinephrine doesn't. You might see this on a test. I'm not sure if I want to leave it in or take it out. The receptor doesn't activate. Beta-2 receptors.
Those are really important when it comes to airway breathing and circulation because beta-2 receptors are located in the lung. Does anybody here have a severe allergy where you need an EpiPen or a Guinness? Where are you allergic to? I guess bumble bees and waspers and what not.
Okay well luckily we barely got grass out there and no flowers so it's not, you probably won't see any of them around here until when spring rolls through really well. But people who have an allergic reaction can go into anaphylaxis that their airway shuts off, your airway doesn't shut off does it? I don't know. I have no idea actually. They told me that I needed one because they did an allergy test and it was like really severe or whatever but it was like...
So please don't do that here. The only thing we've got out in the hallway is narnia. The CT dye I done. I go in the anaphylactic shock because of that too. Okay, so if you went into shock and your airway started closing off, then epinephrine is like the main treatment for that.
You get the epi injection. They don't do norepinephrine because it's not going to affect those receptor sites. Norepinephrine, as a medicine, we typically give for people in shock states, but not anaphylactic shock because it won't be effective. So we have different neurotransmitters that activate, and we have different receptors. Here's a table.
If you look in your McCusden pharmacology book, I'm not sure which table it is, but there's a breakdown of what happens when you activate receptors in the parasympathetic and the sympathetic side. I tried to give you a little breakdown table of that in here, just so it's compiled in one place. Now, for the sympathetic, We have sub-receptors, alpha-1, alpha-2, beta-1, beta-2.
The main thing is where they're located. Beta-1, one heart. Beta-2, two lungs. Now there are also beta-2 receptors in the uterus.
And there are some medications that they can give to help. Say for example, a mom of two babies having contractions early when she should have. Have you all talked about medications to delay or stop contractions?
- Ish. - Ish? Okay, so some of the medications will work through the sympathetic nervous system.
So when you give them, it can delay labor. I don't want to go into that in big details because that's a Mrs. Gates, Mrs. Williams topic. But with some of the medicines that are used to delay labor or contractions, Now, the alpha receptors. Alpha 1 is basically out in the peripheral arteries.
Arms, legs, and the body. And activating them causes vasoconstriction. Next week we're going to talk about preload and afterload.
So when we cause vasoconstriction in these peripheral arteries, it's going to, it just basically tightens them up. it increases blood pressure because the heart has to pump harder to get the blood out. It's useful in some shock states, but this semester we don't like that activation because it increases blood pressure. And some of the medications that we're talking about this week and next week are we want to lower blood pressure. Hypertension is like one of the major illnesses.
in the country, in the world. So we like medications that are going to decrease that tension. So alpha blockers are some that will do that.
So when you activate a receptor, you're going to have an effect. When you block a receptor, it's also going to have an effect, usually the opposite. Does this make sense?
Does the epinephrine not act on the A1 or A2? It acts on all. Alpha 1, Alpha 2, Beta 1, Beta 2. It's going to activate all of them.
So is norepinephrine the main one, though? The epi is the main one. Here, it's just what I wanted to talk about.
Everything, if you go back right here, the epi is going to activate all of them. So here the norepi is going to activate all of them except for the beta 2s. The muscarinic, that activates the heart as well, so does B1, so what's the difference? Okay, so they're in different branches of the autonomic nervous system. The beta 1 is sympathetic, the muscarinic is parasympathetic.
We're going to come up on the dual innervation in a few slides. Look at the locations and what happens when they're activated. So the key thing here, in most of these situations, that when you give a medicine, it activates something like the beta-1. Beta-1 is in the heart. When you activate it, its goal is to speed up the heart, to increase blood pressure.
If you block it, the opposite is going to happen. It's going to slow down. That's why beta blockers are one of the big blood pressure medicines that we use. The alphas, one, two.
This is where some people get mixed up. And I'll try to explain it here and it's definitely coming up again. The alpha one, activating it causes blood vessels in the periphery to constrict. So if you use it about, so it increases blood pressure when those are activated. But the alpha-2s are in a different part of the body, more central.
Activating them actually lowers blood pressure. So this is one of the things that it tricks people up when we get to the blood pressure medicines. Clomidine is a medicine that acts on the alpha-2 receptors. So think more central nervous system on this one.
By giving that blood pressure medicine, we're activating but it's causing an opposite effect as to what happens when you activate the alpha-1 receptors. The reason that I like to give is back in the day, when I was growing up, that parents were extremely controlling, right? Are you still like that, moms?
That there were little parts that they could add into vehicles that it limits the speed you could do. that I could go up to 55 miles an hour driving, but if I hit the accelerator and the gas pedal more, then that little extra add-in that mom and dad had put in kicks off the accelerator's power. That's basically what happens with the Alpha 2 receptors. That I'm in my car, I'm driving, it's like it's the 1980s, it's like Duran Duran is on, I'm listening to Kiss on the 8-track tape, and I'm feeling like running fast down the road. So I hit the gas.
45, 50, 55, and then clunk. It kills down the road. Alpha-2 receptors are basically that little regulator. When in the body, when norepinephrine levels get too high, it kicks in as a stopgap and tells the body to stop releasing norepinephrine. Cut off the gas because you're going to blow valve out.
That's the gist of it. Now this is about the point where I lost the main campus students. Okay? Filling it.
Okay. So we're going to go over it again at the end. Like I said, we're going to be repeating a lot of stuff like five or six times over.
It's repetition is key here. So when alpha one is pressing down on the gas and you're going real fast. Yeah, it cuts off the gas people. I'll do yeah, so what's happening is that?
So norepinephrine is a flooding system. I'm in the car. I'm speeding It's like I've done a lot of diet pills and it's like I'm just feeling like going fast so bam, I am, my alpha-1 receptors, they're kicked in.
It's like norepinephrine is flooding everything. So my body does not want to blow a blood vessel anywhere. It doesn't want to stroke out or do something. So when that level of norepinephrine goes in, like the car going too fast, that little regulator kicks in and says, okay, slow it down. So what it does is it cuts down the release of norepinephrine.
So basically it just, it keeps you from going too fast and blowing up your heart. Does that make sense? - Mm-hmm.
- Okay, I was wondering what happened? - Yeah, so 15 on my phone, but my phone died. - So we've got walk, heart, and blood.
Okay, let's look at the beta-1. Beta-1 is mostly in the heart. That's what we typically word it.
There are some beta-1 receptors in other parts of the body, like in the kidneys. We'll talk more about the renin-angiotensin-albosterone system next week. But there are a few receptors in there that when they're activated, it tells the body to hold onto water because more circulating fluid will mean more. So the whole purpose of the autonomic nervous system either comes down to the sympathetic, what we need to do to get away from flying higher, whatever. Parasympathetic about resting and adjusting.
So moving down to the beta 2, the biggest places that, the ones that you're going to worry about the most are the lungs with beta 2 receptors. There are medications. Does anyone here have asthma?
Do you have inhalers? What kind of inhalers do you have? I have Trilogy. I have albuterol sulfate.
I have a nebulizer, so I get a lot of upper respiratory infections, so they put steroids in it with albuterol sulfate. I'm a chronic asthmatic. Okay, stop that.
I can't, I'll bet. Okay, so one of the magic medications, albuterol. Albuterol is beta-acid. So it's going to activate those beta-2 receptors in the body.
Now, that causes bronchodilation. Remember, we're in a state of needing to get away at this point. So, by opening up the lungs, we're increasing airflow. So, more air in the lungs means more oxygen attaching to hemoglobin, which means more oxygen getting to the cells that need it to escape.
Now, the next part, the muscarinic receptors. See a cold laying there? We're not seeing that in the lion-tiger-bear situation.
We see this after we've escaped from the wall. Back in our house, doors closed, and we're relaxing. So here, heart rate's going to go down.
Secretions to eat, salivation, GI tract motility. Okay, it's like I don't have to worry about leaving the tiger back through a trail of pee. So let's spend more energy with urination.
I pulled this out of your book. In the old Lenny book, there was a table that I loved, but this kind of sums it up. that this is what happens when receptors are activated. On the sympathetic side, those alpha-1 receptors, alpha-2 receptors, beta-1, beta-2s, when those are activated, this is typically what we see in different organs of the body.
The parasympathetic, if you look at them mostly, it's opposite. So in most of these situations, we can say that This can help you pass a lot of the test questions I think in the future. This is what happens with activation. So when you activate the sympathetic, pupils go why? When you activate the parasympathetic, pupils constrict.
Now activating a receptor and blocking a receptor has effects because again, we're working on balance here. I'm going to wait, okay? I'm going to wait. But for the most part, when you activate this parasympathetic response, here's what happens to the pupils. If you block that receptor, then the sympathetic is going to take a more active role, and it's going to lead to pupil dilation.
So this happens a lot with the side effects. So if you know what's happening when a receptor is activated, then by blocking it, the other part of the system has a more pronounced effect and you get that as a side effect. So, lungs.
If I am, okay, so with your albuterol, we're activating those beta-2 receptors in the lungs and we expect those bronchioles to open up so you have better air flow. Now, Let's say that you are an evil nurse, and this person that's in the hospital that needs albuterol, not you. We like you. We don't like some other people. So we're in the hospital, and this is somebody you know.
You don't like them. It's like in kindergarten, they took your crayon, your favorite crayon, and you held a grudge for 40-plus years. You're their nurse, and you want to kill them.
You can give them something that blocks those beta-2 receptors and what's going to happen? They're not going to be able to breathe. Right. It's going to cause bronchial constriction right here.
So, again, activating something right here has an effect. Blocking it typically has the opposite. And it's the same thing with the receptors.
Now, the receptors. alpha-1, alpha-2, beta-1, beta-2. The muscarinic on the parasympathetic side has different little breakdowns.
It has M1 and 2 and 3. Technically there's an M4 and M5, but we're going to ignore those until much later in the program. There are nicotinic receptors, but nicotinic receptors come along mostly with neuromuscular disorders. Doesn't tie into the blood pressure stuff that we'll talk about.
And again, 54 weeks, this is when we'll talk about the nicotinic receptors. Those are mostly at the neuromuscular junction and they're typically affected in a disease called myasthenia gravis where the body destroys them leading to the inability to contract skeletal muscles. Okay, tell me what questions you've got right now.
On the last slide, you said the sympathetic does what, but the parasympathetic blocks it? No, no. They're two separate things.
So we've got this sympathetic, this parasympathetic. Have you all watched Avatar, the last airbender? I think the two systems lived in harmony until... So what happens is when you have the pupils...
We have, what's a good, let's say that we have a disease like glaucoma where pressure builds up in there. So we need to cause those pupils to constrict like this so that fluid can flow out. We can do that with different kinds of medications that affect each system.
So here with the sympathetic, would we want to activate those receptors or block them? We want to block them. So both activating is going to make them open wide. So if we block those receptors, they're going to close up. Now the opposite side, the parasympathetic, do we want to activate those receptors or block those receptors?
We want to activate them because that side, we don't need to see all that stuff. It's distracting, closing down. So we've got two systems that kind of work almost opposite each other. So there are the overall drops that are going to affect the sympathetic side.
And then there are some cholinergic ones on parasympathetic side. Confused yet? It's getting worse, isn't it? Hopefully, the main campus kids understood most of it by then. So I'm going to guess you guys will too.
On the test questions, will it be like, will you give us a scenario to see which one we activate and which one we don't? Okay, so it varies. I did your test question.
I still have to review and rewrite some of them, but there are a lot of questions. I'm not going super complex on this one for you. So it would be like what you kind of just asked.
So my niece went through a master's program at Marshall University. And she sent me the, like when she had this lecture, she was texting me and asking questions. I'm like, send me pictures of those practice ones. And they were a lot simpler than I used to ask.
So I toned them down. So mostly, you're going to see a whole lot of, okay, you activate something happening. I understand. I'm falling asleep and I don't want to make a selection.
I fall asleep anywhere and everywhere. It's like a problem. Would you like a fry?
No, it's okay. Thank you, Dave. I can't have my caffeine.
So what you're mostly going to see on a lot of these questions is, okay, so you activate a beta-1 receptor. What is going to happen in the body? So if you see a question, it's like, okay, you give a medicine that activates beta-1 receptors. What are you going to see?
What organ is it going to affect? The heart and kidneys. We want to see the heart and sometimes the kidneys because we want to increase the blood pressure.
Okay? You see another question? It's like, okay, we're giving a beta-1 blocker. It's going to slow the heart.
We give something that activates beta-2 receptors. The lungs. The lungs. But if it's activating the receptor, that's the sympathetic response.
And then if you block it, that's the parasympathetic response. Well, yes. So what happens is that in the lungs, it's dual innervated.
So it has attachments to the sympathetic and the parasympathetic. So if you're blocking those beta-2 receptors, we're decreasing that ability to have. So the parasympathetic side kind of like picks up and their whole goal is to constrict stuff. We don't need to run.
We don't need to. So let's say I'm like dying of an asthma attack, okay? And obviously you want to activate the beta-2 receptors to open up the bronchial spasms, like bronchodilations.
Uh-huh. If you don't want that, that's the sympathetic response, right? Yes.
So you don't want that to happen. The opposite of it is the parasympathetic. So you would want to do a beta-2 blocker.
No, no, no. We want a beta agonist. So a beta agonist is going to activate those beta-2 receptors.
That's what albuterol is, a beta agonist. Yeah, yeah. So by activating those, those bronchials open.
Open, safe, and brief. Yes. But what if you don't want that?
What if you want to kill them? If you want to kill them, then you give them a drug like propranolol. So the parasympathetic.
If you want to kill that person, you're going to give them something that's going to cause bronchial constriction. Propranolol is one of the drugs that we always talk about in here. Would that be considered a beta blocker or agonist? That's a beta blocker.
Okay. So remember, agonists, you want to open up the lungs. Beta agonists, open.
Beta blockers are going to close. Block. Oh boy.
This one gets kind of, it gets tricky. For some reason in my mind I thought the beta 2 agonists were the blockers. No, those are going to activate beta receptors.
So that's going to increase heart rate for beta 1 and open the bronchioles for beta 2s. Okay. It says on this chart, it says for the cholinergic, like parasympathetic, it says main location is heart, gland, smooth muscle, and detrusor. Are those the only places or are those just like your main ones? That's like the...
We lecture, we're talking about the main locations for these things. Like the alpha-1 receptors, they're mostly in the arteries. They're a little bit in the heart too, but the beta-1 has more.
Think of it like the classes here. So we would say that, okay, nursing classes, mostly females. but you're still some meld here. So if I say ladies scream, scream. Really?
Really? It's gonna be a lot more squeaky here. Yes, it's like so if I'm activating the female receptors, it's like there's gonna be a more pronounced spot here compared to engineering which has more men in it than women.
It's like a flip. So we worry about what's happening with the main receptors in those locations. I have another question.
What's the difference in the agonist and the receptors then? I feel like that is a dumb question, but I feel like I should know that. So agonists, it's like, an agonist is like the epinephrine.
It's what flips the light switch on for those receptors. If you think, you can think of like the receptors like little light switches. The It's like, ooh, there's a lion. I don't want lions and tigers and bears because I watched Wicked last night.
It wasn't really family-seeking, but still. So I was like, ooh, there's a lion. Okay, so beta-2 receptor.
Okay, the lion wanted nothing to worry about, so I'm calming down. Less epinephrine, less activation. So the receptors are basically switched like an on and off switch.
So an agonist is going to flip that switch on and activate it. And then when that epinephrine or more epinephrine or whatever decreases, it just kind of like flips itself off. So whenever you activate the receptor, that's the sympathetic, it calms down or you want to block it and it's the parasympathetic? Not quite. Oh my God.
Because you've got two systems. I'm going to shut up now. No, no, no.
You've got two systems. I think you're seeing it as one thing, but it's two divisions. Yeah. So what's going to happen is you can give that beta agonist that's going to have an effect, but you also have cholinergic medications that are going to have an effect. Okay.
with the breathing, I can give a cholinergic medication when it activates those parasympathetic receptors. So that's what it calls bronchial constriction. So just think of it as like two siblings that they always do the opposite from the other one. This one wants to breathe, this one's like shut up you're talking too loud.
I'm hoping it'll get better. I said the main campus got it so you got I think you guys are a little smarter than them or they were just real quiet. All right so the receptors. The key thing here is you have to remember which side is parasympathetic and which one is sympathetic and knowing what happens when you activate one on each side.
The subtypes. Here is Morton Merv. I think this is from one of your old pharmacology books, but I like these guys.
The subtypes are helpful in tailoring the response. So here, if we have Mort here, he only has receptor types A, and the brother Merv has four different types, A, B, C, D. So if we want to give a medication that activates that receptor A, just making this up as I go here. So if we give that medicine to Mort, then all of his receptors are right. He's going to get a faster heart rate. He's going to get increased GI speed.
So he's going to get diarrhea. We're activating those receptors in the bladder, so he's going to pee himself. In his hands, he's going to start flapping.
So his brother, who has more receptors, is going to have a more specific response. So here, if we give that same medicine here to Merv, then it activates receptor A, then his heart rates are going to go up. He's not going to have the other problems that the brother has. That's how specificity and picking medications that have certain receptors basically what we like to do.
The lungs are a good example. So we're going to talk some about the OLAW drugs in a little bit. The beta blockers.
So Morton Merv here, if one of them has high blood pressure and they have to have a beta blocker, there are specific ones that target beta 1 receptors or there are general ones that attack both of them. So picking the medicine that is specific to better blood pressure is the better choice because it'll slow the heart rate, but it's not going to affect the lungs. The propranolol is the generic one or the general one that affects all of them.
So in addition to lowering blood pressure, we're also going to cause some bronchial constriction. Could be bad in somebody with asthma. Has the mud cleared up a little bit? Yes, it has.
Okay, so again, this is why we like medications that target certain things. On this slide, like let's talk about blood pressure since that's what we're going to explore. We talked about that a little bit long ago. But what if we used a medication that affected alpha-1 and alpha-2 receptors? What did the alpha-1 receptor activation do?
Increase blood pressure. It increases blood pressure by constricting the arteries. Vessels.
Yeah, it constricts the vessels out in the blood. What does alpha-2? Lower the blood pressure.
It lowers the blood pressure. So if we're given a medication that is activating both of them, it's defeating the purpose. We're not going to have a really great effect because we'll go one side and say lower the blood pressure, but another one saying increase the blood pressure.
That's why we try to use targeted medications like some of them that only affect beta 1. If we use, I'm sorry, alpha 1. If we give something that blocks alpha 1 receptors, we're going to decrease blood pressure because by blocking those receptors, the arteries open up and it decreases after. Are you okay? Main thing, we're going to get to the medications on the test. You are going to see side effects and stuff.
So let's use albuterol again as an example. How often do you use an inhaler? Too much.
Too much? Yeah. How many times a week? I probably like once or twice a day.
Oh, you're too much. Yeah. I have really bad asthma. Yes, that's...
Like a nerd. Yeah. Bang.
Tell your doctor you might need some medication changes done. Rescue inhaler, you shouldn't be using it once in a while. No, that's why I need to use my nebulizer.
So when you use that for say the second time a day, do you have any side effects? How's your, do you feel palpitations? - When I take my nebulizer, I feel like I'm going, as weird as it sounds, almost like I shake really bad, like I can't hold a pencil or anything. It's hard to concentrate 'cause I'm shaking so bad. I feel like I have palpitations.
- Is albuterol in there? - Yes. - So, albuterol, some of the main side effects you get with that are, some people get palpitations, like they're increased heart rate.
because it leads over and activates the beta-1 receptor. It's activating those little beta receptors in the muscles that cause tremors. I do that really bad with my nebulizer. Not really with my inhaler, but most of the nebulizer. So does the beta-2 cause muscle, like skeletal muscle contraction?
Yeah. So what happens, because it's active, it plays a part in you having to get out of there. Remember, you're running from the lion, tiger, and bear.
So, the albuterol, that would technically be an agonist then? Yes. Albuterol is a beta agonist. That activates the beta 2 receptor. Yes.
Okay. Good. Y'all are reaching wide over here. You're going to pick up a pace though.
She's not making eye contact, so you're going to be next in line. Okay. Now, medications.
I added some hypertension medications into your unimaterial pulpers, so be sure to look at those before next week or before the test. Now, just again, this is where things are mostly laid out. Similar walk we had before, but the medications that we were using. The phenylethrine.
I mean, you have sinus issues. Do you ever use the nasal spray? Like in the morning, when I can't breathe through my nose.
Okay, so phenylephrine is one of the main medications that they use in nasal sprays like that. It activates the alpha-1 receptors, which causes what? Dilation or constriction?
Constriction. Constriction. We're activating those receptors. So it causes the vessels in your sinuses to constrict.
It opens up the airways. Did you say the butamine? What is it? What was the meditation you said?
Phenylephrine. Oh. What are you looking at?
Butamine. Oh, no, butamine we're not going to narrow this semester. That's another one that you'll talk more about in shock. I mean, we can if you want to. OK, so clonidine.
So clonidine is the blood pressure medicine. It activates those alpha 2 receptors. And that's going to decrease the production of more epinephrine. So it's going to decrease blood pressure that way. The dobutamine, okay, so we're dobutamine.
It's one that we use when a person has like a certain type of shock and the pressure is too low. So by activating that, it's going to increase cardiac output, increase blood pressure up. Talked about metoprolol, talked about yalbutol. So if you've got any questions.
I know we do, so don't be afraid to ask them stupid questions today. This is, like I said, this is one of the trickiest ones just because you have two branches of a system that work in different ways, that do opposite things. So how does the alpha-2 receptor, how does that, like its stimulation, like lower blood pressure?
Okay, so when, say for example, it's norepinephrine levels in the body are going too high. then this gets activated and decreases the production. I'm pushing the gas pedal too fast, the little regulator says, "Ah, you can't." It cuts off the flow of gas to the engine.
I want cars to slow down some of the stuff. Now, that's the sympathetic side. Parasympathetic, rest and digest.
When we start looking at these, who here loves their Benadryl? What does Benadryl do to you? Makes you sleepy. Makes you sleepy.
That's because it is like one that hits all of these muscarinic sub-receptors. The little sub-receptors are kind of spread out in different spots through the body. So, like right here, the cognitive part.
Muscarinic root bone receptors are kind of located in the central nervous system. Messing with those, we get sleepy with the Benadryl. So it has anticholinergic effects.
We're going to talk about Alzheimer's medications in unit six. But just for now, know that when we're talking about like Alzheimer's and Parkinson's, usually there's an imbalance in acetylcholine levels in the brain and gut. So increasing acetylcholine levels helps with Alzheimer's in the early stages. not greatly slows the progress of memory loss over a short period of time.
So M1, we look at the brain. The M2, we have that a lot in the heart. So activating M2 receptors will do what to the heart rate?
Yes. Because it's about rest and digest. So it's going to slow the heart rate. Atropine is a medicine that blocks those receptors. So for blocking that, what's going to happen?
Speeds it up. Speeds it up. Have you seen heart atropine given in the?
No. Okay. So yeah, I didn't know. Stop the heart.
Yeah. So yeah, atropine is one that will block those parasympathetic receptors in the heart that says slow down, and it'll allow heart rate to go up. So we use it for things like bradycardia.
Is it an anti-hypertension? Now, here the M3, when we're talking about this one, this is a lot of the GI stuff. So, and gentile urinary. The one that I've usually talked about in the past has to do with the bladder. So when we're activating those receptors, now the detrusor muscle is basically the big bladder.
It's like the bladder wall. So when you're activating those receptors on the bladder, it's saying squeeze. So it's used for problems like urinary retention. Since we're talking about OR and the operative stuff, that sometimes people who are post-op have trouble peeing.
So this is a medication that can be given to instruct the bladder to contract. Now on the flip end of lock-in, we have anticholinergic medicines. What is that going to do? Prevent bladder spasms? Yes, it's used to treat bladder spasms.
So it's blocking his receptors. So little Nana who has to go to the bathroom every 10 minutes, it's blocking his receptors. So instead of getting like that twitchy bladder, it's allowed to feel more. So she has less need to go to the bathroom every 10 minutes.
So cholinergics are going to make her pee. anticholinergics are going to make you retain urine. Now, in the elderly that is a big problem sometimes.
Benadryl in elderly people, especially elderly men with prostate issues, it can lead to some significant urinary retention in those little men because it affects parts of the prostate that should relax and it decreases the ability of the bladder to constrict. It's also what causes dry mouth since it's attached to the GI tract. If a patient comes in on these medications and they have dry mouth, what are you going to do? What did you ask? If somebody's mouth is dry, you give them water.
Okay, drink more water. Here is an in-spray. It's like here, chew on some sugar-free gum or something to help increase secretions.
The GI tract. What will a medication like the Danacol that activates muscarinic receptors do in a GI tract? Faster or slower?
Faster. It's going to go faster because the parasympathetic and cholinergic is all about rest and digest. So it's going to increase salivation. It's going to increase movement through the tract. What is it going to do to the lungs?
Slow down your heart rate. Yes, it'll slow down the heart rate. Is it going to make you breathe more?
What about the lungs? Is it going to make you breathe more? When you say breathe more, do you mean... Increased respirations?
Do you mean bronchial constriction or dilation? Honestly, I don't know. I get them confused.
Okay, similar. When you say don't breathe as much, I don't... Constrict means like they open and close more frequently.
So parasympathetic activation is about rest and digesting. It's closing those frontals. So you being asthmatic, what if I give you bethanacol for urinary retention?
What will happen to your lungs? They constrict. They'll constrict.
So it might trigger an asthma attack or some symptoms. So we really ought not be doing it. Now if we go back to one of Mrs. St. Clair's lectures for Bethanacol, they were investigating a few years as a treatment for GERD because it increases motility through the GI tract.
Instead of things backing back up, it helps move it through a little quicker. But it affects the lungs. Yes.
It'll cause bronchial constriction. And why does it cause bronchial constriction? Because it's activating the parasympathetic side, those muscarinic receptors in the lung that are all about rest and digestion. Those floor receptors are getting signals like, okay, we don't need a super lot of oxygen right now, so let's shut down some bronchia. So all of these can counteract Yes, so this way if we're giving so you have albuterol and That activates the beta receptors that says open up, but if we're given another medicine that says okay close the bronchioles down then we're decreasing the We're kind of fighting each other there one say it open one says close so that drug is a, I don't know how to say it, is it atropine?
- Atropine. - So could that do the same thing, like counteract the albuterol, since it's an old, allergic drug? - So, well, what does it do?
Is it atropine? It's a blocker. So it's not activating those parasympathetic receptors, it's blocking them. - Oh, okay.
- Now we'll talk about that a little bit in a few slides. So we have to know what the receptors are, where they're at, what happens when they're activated, what happens when they're blocked. That's one of the key things you have to pick out in this. Now, the dual innervation.
Some of the organs have attachments to the sympathetic and parasympathetic, meaning that each branch of the system can have an effect on that organ. The ones we really worry about are the heart and the lungs. Next step would be like the GI in the bladder and the eyes for, I think, a deafness.
Do you all need to stretch before we talk? Do a stretch. I find it most confusing because this is where we have beta-1 agonists activated to speed up the heart rate, but you also have the parasympathetic inhibition with the muscular nerve receptors getting activated to say, slow it down.
So in these dual innervated organs, it's usually like a flip situation. That if you're activating on one side, it usually has the opposite effect of activation on the other. Now here, back to the liver. We talked about this a little earlier.
So it doesn't have dual innervation. There's nothing rest and digest wise that says there's an emergency. There's no process in the the body for rest and digest that says, okay, there's an emergency to go ahead and start building up another process in the body.
Same thing with arterials. It's like we don't have a lot of, there's no need for parasympathetic innovation because the main thing for the vessels is activating to increase blood pressure. So once that epinephrine or epinephrine starts flowing, then they start to relax again.
There's no need for parasympathetic innovation. Does that make sense? Yeah.
No, you're saying no, you need to fib. Fib. But it's okay.
No, I thought I understood it. Okay, good. You did not fib.
Now here, there is a typo on your slide. I think this a beta one activation or something on. So that's typo. Good. I'm glad you called it.
Because I was watching it. I did this over spring break and I was like watching TV and the cats were needing attention. And I wanted to play my game because it was your time to reset to get more diamonds.
And it's just a busy moment. I used a copy and paste and I forgot to update. It's not supposed to be activation, it's supposed to be blocking.
Yeah, the slide up here is correct. So when we talk about dual innervation in the heart, this is what happens here. So when we activate beta-1 receptors, it increases the heart rate.
It increases your blood pressure. When we block them, it decreases the heart. So on the other side with the parasympathetic, it's just flip-flopped.
So the parasympathetic activation increases? Parasympathetic? No, decreases. Oh, okay. I didn't know if that was a typo as well.
No, no. No, the head is where the autopsy was on. So here we've got, it's just like a big... X or zigzag here that we activate beta-1 receptors you're getting the same thing as when you block parasympathetic side. So it just kind of flip-flops there.
So as long as you know what beta-1 activation does and like sympathetic activation in the heart, then it's the opposite of parasympathetic. Same thing with the lungs. The cholinergics are going to cause bronchoconstriction, anticholinergics, bronchodilation, beta 2 activation, bronchodilation, beta blocking, bronchoconstriction. So you've got to remember that it's like flip-flops. We're going to talk about some mnemonics.
So when we're talking about sympathetic, it's all about stress, speed, and strength. That's what happens when that gets activated. Parasympathetic, pee, pooping, and the other pee, it's like producing secretions. And secretions usually, it's like the GI-related stuff for the most part. The salivation, all the stuff that you need to get that french fry from the gut.
Eyes. It helps increase like... the flow from the tear ducts. Keeps your eyes moist.
Alpha-1, arteries, beta-1. Beta-1's where? One heart, two lungs.
Now, the toxicities. The boards love little mnemonic things like this. So, we have some scenarios that are coming up.
We're going to talk about the dumbbells and the Mazda hat. These are things to help you remember Like what happens if you get too much of a cholinergic medication or too much of an anti-cholinergic? Right here. Thanks to being the image creator, now renamed as Code Violent, we can update the fun pictures on our slides. So you tell me, in the man who was dumb enough to wear dress shoes into a jungle, What side of his autonomic nervous system is being activated?
Right. Sympathetic. Parasympathetic. Sympathetic. That's a nice one.
I heard different answers. Let's settle on... Sympathetic.
Sympathetic. By her flight. So, he is flighting right now. Neurotransmitters.
What neurotransmitters are flooding his system? We've got... Epinephrine or epinephrine. Epinephrine or epinephrine. Okay.
So tell me about the fact, what are those activating? Which receptors? Alphas, betas, or muscarinics?
Alphas and betas. Alphas and betas. What is the alpha-1 activation doing in the body?
Increasing heart rate, opening the blood vessels. Alpha-1 activation. Instricting the blood vessels.
You're on the right track. I think I hear what you said exactly. Constricting?
Constricting. So, because it increases blood pressure. Beta-1 activation is going to do what? Alex, this is yours. Beta-1 activation.
What's it doing? It's going to speed up the heart rate. Speed up the heart rate. All right. So, increasing heart rate, increasing arterial constriction, we're increasing blood pressure.
What's happening in the liver right now? Remaining the same. But what's it releasing? Glycogen. It's breaking down glycogen to make glucose because the muscles have to have energy to run.
Respiratory. What's happening in our lungs? Constriction. They're dilating. Because it's opening up the airways to get more oxygen in.
So in fight or flight, it opens the airways? It opens the airways. Why does it feel like it's constricting them?
when you run out of breath that's just when you're tired yeah thank you so what were some of you i'm just here let me just say bad words in my mind maybe just a weak ass tired no it's just that's that's just the the way the body what happens is it's that you get tired but you're you're your bronchials are still open so With, so just relating to the picture, with the Alpha-1 would be just using like physical attributes. So let's say like a muscle, think of it like a muscle constricting and then you know when you run obviously your lungs expand. Is that kind of like what you're saying? Yes. Okay.
Now in the Tiger, he's in fight mode so his would be similar. Now the next one. The tiger won.
I'm parasympathetic. He chewed up the man in the polycotton blend in the war and got him a circle. So what's happening with him? Parasympathetic. What is what?
Parasympathetic is activating. So neurotransmitter for that? Acetylcholine. Acetylcholine.
And the mucirin receptors getting activated or doing what? Let's see. Eyes.
Bigger. They're smaller than you. constricted. He doesn't need to see all that stuff anymore.
So they're going from, they went from here earlier to here. And his heart rate's like decreasing as well? Heart rate's decreasing. GI tract is speeding up or slowing down?
I'm speeding up. GI tract is speeding up. Does he have to pee?
Or should he have peed already? He'll have to pee soon. And the A nice little flower above the ear.
It shows how relaxed he is. Oh, she. I don't know how to talk gender in pictures.
Okay, so you can see the differences in what's happening in the plot. Now, another way to remember, since we were all about vehicles and stuff this time, is if you're thinking about the sympathetic nervous system, think of it kind of like a car. That you need to go fast, you hit the accelerator.
You're activating like the beta-1 receptors in the heart, for example. It's speeding up. You turn in on the air conditioner, so you've got more air flow. Those are the big issues that we deal with when we're talking about the sympathetic nervous system. So here, when we're activating the beta-1 receptor, one accelerator, one gas pedal.
So press it, speed up, block it, slows down. The air conditioner, I mean my car has more than two vents on it, but you can only go so far when you're making stuff up. So, air conditioner on, you're opening the vents up, blocking them, less air flow. Basically, one of the ways you can...
Do we have to know the blockers? Which ones? Any of the names of the blockers? Yes. If we look in the bottom here, so for this one, I told the main campus kids that there are some slides with blood pressure medications and a few other things highlighted.
Those are things that you really should look at in your form book. But here, so the O-Lols, metoprolol, or metaprolol if you're feeling it. That's specific to the heart, so it slows down the heart rate.
For Pranavod, it's a non-specific. It slows both of them down. The parasympathetic, the plumbing in the house, parasympathetic plumbing.
We're talking about fluids, pee, and poop. Now, medications. Rest and Digest is?
Sympathetic or parasympathetic? Parasympathetic. Parasympathetic.
When we're talking about medications, you're gonna see lots of different terms. So just remember a few of the key things as we're talking about, and it's like we're in general, either activating or blocking, agonists or antagonists. The terms you might see are going to be varied. You're gonna see paracetamoletics, paracetamometics, cholinergics, cholinomimetics, So the key thing is knowing what the key part of the word is.
Sympatho will be sympathetic. Mimetic means copy. So it's going to copy the effect of acetoporin. Lytic, basically break. So block.
So parasympatholytic is going to block the effect of acetoporin. So methanocol, a parasympathomimetic, activates those muscarin receptors. Once you get the parts down, the agonist, antagonist, memetic, lytic, it's easy. How are some of these medications listed twice?
Because mostly it's just the words. The paracetamol, it's the same thing as methaminus. The only real difference here is where you see the cholinesterase. If you see erase on something, it's usually an enzyme. So cholinesterase, it's an enzyme that eats up acetylcholine.
So if we give an acetylcholinesterase inhibitor, if we're inhibiting that enzyme, it's going to increase the acetylcholine level, which activate which receptors? parasympathetic. Parasympathetic. The ones in red, is that the ones that we need to go into our pharmacology book?
Yeah, those are, let's see, one, two, three, four of them, I know are test questions on here. That's red? That's red. I mean, at least four of them.
Like I said, it's been a couple weeks since I did test questions, so now, the Other here, we've got one side and the other side. Yes? You said if it has the rice in it? It's typically an enzyme.
So on the test, you're going to be giving us the drugs, but not the terms, correct? In some of them, to be fair, in some of them, I might say that it's like what they call muscarine cagumas. So you will probably tell us which term it is?
Partially. I'm not going to say every one of them. I'm just trying to figure out what's the best way for me to learn it.
Like if I should learn the terms stronger or if I should learn the drugs and its purpose stronger. All of them. Yes, but I was wondering which one I need to focus on for study purposes.
All of them. Whichever works best for you. As long as you know that methanocol activates muscarine receptors, it doesn't matter if, I mean...
parasympathomimetic or muscarinic agus. They both mean the same thing. So is there going to be like a curveball and one of those are highlighted as one to be on there?
Or is it? Are you going to treat this? For this part, yes.
There are some medications like the prososin that might come up in next week's lecture. But Typically for this, what I've got highlighted is what autonomic nervous system are. So here, it's the same thing between, it's the same thing. Lytics, memetics, agonists, antagonists, blockers. - You just said methacholine, as long as you know methacholine is what?
You spoke really fast. - Bethadacol. It activates muscarine receptors. The what?
Activates muscarine receptors. That's just an example. You should also know that propranolol is a beta blocker. And I told the other group, it's like you're going to see all kinds of different terms. We have doctors from all over the world and in their medical school they might use a parasympathetic whereas with AA It's about the agonist.
The doctor I used to work with, she learned British English and esophagus started with an O. Anemia had an extra A in it. So you're just gonna see different things. It's important what the words mean. It's basically, it's either blocking the receptor or activating the receptor.
So the cholinergic drugs, they're either gonna activate those receptors and block them. The acetylcholinesterase, stops the breakdown of acetylcholine. So if we're stopping the breakdown of acetylcholine, does that mean we're going to have a more pronounced parasympathetic effect or a less pronounced parasympathetic? So if we block them? If we block, if we get, if we do away with that enzyme that's eating up acetylcholine.
Do you want to be parasympathetic? We're going to see a more pronounced parasympathetic response. And you'll see that again in 52 weeks. Now the drugs, the myasthenia gravis is going to be later. The cholinesterase inhibitors we're going to talk about next unit.
So I'm not going to hit those very hard in this one. The ophthalmology, ilacarpine is one of the drugs that's used with glaucoma. So I think I've highlighted on another.
I'd like you to know what it does. The methanicol we've talked about. the anticholinergic overdose, the physiostigmy. So if we know that anticholinergics do certain things, by logic is what do you think physiostigmy is?
- Like acetylcholine? - Yeah, it's gonna activate. If we have something that blocks acetylcholine, then we give a medication that's going to I see a bullet, so yes. I have a question.
You were just talking about how we would touch base more with those, the next unit exam? Yeah, the dementia is unit six. The ophthalmology, the filocarpine, is that the one that you said that what you wanted us to know more about for this exam? Yes.
because I think I highlighted on a previous slide, the we use it in glaucoma and Mrs. St. Clair will talk more about you with that in the future. But for here, you should know the basic effect it has. And the Bethanol? The Bethanocolin? We do need to know that too, right?
Oh yeah. Because that's also in our reading list. Like we have to know the whole clinical judgment. Yeah. Okay.
Okay. So on cytobats. So we know that the drugs that activate these muscarinic receptors are going to enhance the rest and digestion part. So with bethanacol, the problems that can come with it, it's activating parasympathetic receptors in the heart also, which is going to do what to the heart rate?
It's going to lower the heart rate. So by lowering the heart rate, we're going to increase the risk for hypotension. Diarrhea is because it speeds up the GI tract. The pythocarpine, the glaucoma and dry mouth. I had this one because when I was working at the health right, there was a patient that came in that was complaining of dry mouth.
Dry mouth, dry mouth, dry mouth. And it's like, he's a specialist and the specialist prescribed PO polycarpy and I'm like he's already prescribed it. It's like this is what we would have done.
It's like there's nothing else that I can give you other than say swish out with water or get one of the spray salivas. He's like why do you want to take that because it's side effects. So if we're talking about a pill version What's it going to do to his, since he's getting dry mouth, we know that it's going to increase salivation. It's going to increase GI motility. And it's like, it just was, it's like, well, I don't want that.
I'm like, that's the only thing that we thought that we could give you. It's like, what are you going to do? So do both of those drugs affect the GI tract? Yes. So here, the pilocarpine can increase GI transit time too.
Okay. Now, the toxicity. I don't know if the boards will love it this time.
They have like a 15,000 question test bank and growing. But they typically like to see stuff like this. What are the signs and symptoms that you can pick up on as a nurse? Now, so cholinergic toxicity is one that happens more commonly in our area related to pesticides.
So acetylcholinesterase, It's an erase. So it's an enzyme that breaks down acetylcholine. So organophosphates cause cholinergic parasympathetic symptoms because the body is building up too much acetylcholine in the little synaptic gas.
So side effects just from what we've talked about so far, organophosphate poisoning, parasympathetic overload, what's happening with pupils, Diolating. No, parasitetic. They're constricting. Constricting. Mouth.
Wet or dry? Dry. Oh no, it's wet because you're digesting.
Too much acetylcholine hitting those receptors. GI tract. Constipation or diarrhea? Diarrhea. Diarrhea.
Now here, the... We'll talk about the alternatives. Mushroom poisoning. Not super common here, but they're... How many people are going searching for Bollywood shoes?
Who's that in the woods looking? Have you ever picked the wrong ones? Oh, yeah. Did you eat them? No.
Never? No. I mean, some of those will make you see God.
I mean, other ones will, like, kill you with diarrhea, but... So a lot of people go out and they go hunting mushrooms. And there are poisonous mushrooms in here. One of the vegans is like having to eat a muscarine or something.
The red cap that has little like, looks like oats on them. Have you ever eaten one of those? - No.
I grew up in Poconawas County picking them, but I had a horticulturalist that knew how to look for different types and so he taught me all about them. - Okay. So there are some mushrooms that have a version of muscarine. and muscarine activates muscarine receptors. So we're gonna see an overload of that in some people that would do this.
We don't see sarin gas here. It's like I don't think that Bethlehem, West Virginia is gonna be a high sarin gas terrorist target. But you might see something like that in the boards.
I doubt it, but you're more likely to see something along the lines of pesticides. So cholinergic toxicity is where the dumbbells come in. And it's just that little mnemonic that helps you remember. The diarrhea because we're amping up the GI tract, urination because we're telling the bladder to get strict, the meiosis, meiosis and mydriasis, little word, little pupils, big word, So little pupils, bronchospasm, the heart rate is going down.
The amnesia could come from like the overactivity of the GI tract. The lacrimation is the wet tearing eyes that happen. Lethargy, it could be hitting those little receptors in the brain. Salivation, wet doggy type drool, like the We used to have a St. Bernard.
That's like that dog was 90% spit. So you're going to see a really wet mouth. Now, the anticholinergics are going to do the opposite.
So here you're going to get the dry stuff. The atropine is one that we've talked about. What is it going to do to the heart rate?
Speed it up. Speed it up. Now, the oxybutynum, it's one they give for the spastic bladder, the little men who have trouble with leakage or urinary frequency. The scopolamine is another one that we talk about.
I've thrown this one in on the tests in the past because they used it in hospice. I don't think it's as common now, but in the past, they used scopolamine for people who are near the end and they've got these really burly secretions happening. Well, this helps dry those up.
It just helps with the motion sickness in the mouth. You should know that as a clinical emergent, it's what causes dryness of the mouth. What to the bladder? - The dip.
- Okay, so case study. So if you're a male, hernia repair, hasn't been able to urinate for the past eight hours, Feeling strong urge. Extended bladder, abdominal discomfort. Okay, so the thanacol, what is it going to activate receptor-wise? Alpha, beta, or muscarinic?
Muscarinic. Muscarinic. What's that going to cause the bladder to do?
Retention. Relax or squeeze? We're activating the muscarinic receptors on the detrusor. Squeeze. What are some of the side effects that the nurse should look for?
You. You're the one that's watching this patient. No, not dry.
We're activating the muscarinic receptors, so instead of dry, we're going to get wet. That's what happens to the lungs. Bronchial dilation or constriction?
Constriction. Tachycardia or bradycardia? Tachy.
Perfect. Hypobal sounds or hyperbal sounds? Those two were too close.
I'm going to pick hyper. Hyper. Okay. So, the ones that usually get things like this are... To be honest, the people who are the little nanas who are taking the bladder medicines and Benadryl.
One of the biggies that get the symptoms like this. The next are people who are taking like psychiatric medications. We'll talk about these when we get to psych and Ebola. But the tricyclics and the antipsychotics, all of them really strong anticholiner.
Now the last, look I told the ones down in the main campus that's there it's been several years ago that there was a little kid that came in that had eaten at Jimson every day and he fit the symptoms that are coming up pretty closely that I don't know what happened to him it got transferred out of Raleigh Journal assuming he made it I didn't recall seeing anything in the obituary but I'm nosy like that I'll look up patients name and check the obituary it's like a few years ago one of our students missed something really big and said, "Let's just check the obituary for the next few days." So for like a year and a half I'm like, "Did she show up in the obituaries yet?" Where were you working when the person ate all the gypsum weed? Up at Raleigh General. I was in the nursing special care nursery. I was a little kid. So some of us got called down.
That's like nothing I could do. But they were like in case they needed like an IV. And there were people that worked in the nursery for like 20-something years or 30 years.
And it's like I'm there for a year. But I'm like, I want to go see this too. And no babies were birthing.
But the things that you saw with it, We're kind of like this. This is where the next mnemonic comes in. It's like hot as a hair, they've got a fever, red as a beet, they're red and flushed, dry as a bone, dry mouth, no heat, dead blind as a bat.
So the meiosis, little word, meiosis, little pupils, mitriasis, bigger word, bigger pupils. Now, the cycloplegia, I don't know if you'll see this. You won't see it on the test.
But basically, it's like a little temporary paralysis of the muscles that help your eyes accommodate. When I'm looking here, and then to Alex. Then here, then to Ricky. Here. It's like there are little muscles that are like...
like change the shape of the lens in my eye. So it makes it a little harder to see because there's different focusing. The maddest hatter, I don't know, the kid was too young to read. But it's like these people are like you.
They're not typically oriented fully to person, place, time, and situation. Now, just to compare the two, put them in a table for you. So you can look and see really quickly what to expect. Okay. Case study.
Now, this one has the answers on it, so work through it really quickly. We have farmer, emergency room, abused, vomiting in the field, spraying insecticides, and collapse. Okay. So in the vital signs, what supports a cholinergic crisis? The heart rate.
The low heart rate, and we have a lower than normal blood pressure. So that comes from... the parasympathetic stimulation in the heart. It's telling the body to, it's resting time. So let's look.
Yes. So what's happening in the lungs? Constriction.
So we've got an increased respiratory rate. So the physical exam pretty much goes along with what we see. Constricted pupils, salivation, bronchospasm wheezing, diarrhea.
It's that classic dumbbell stuff that's happening. I have a question. So what's the difference between a cholinergic problem and just having an adrenaline rush for an emergency? Oh, well, typically we don't get, with an adrenaline rush we would see bronchodilation. the pupils would be larger.
Diarrhea, urinary incontinence, the GI tract would be slowing down and the urinary sphincter would be clenched on that. So we would see different symptoms. So here, the treatment, what we've talked about atropine, We haven't talked about the Tupan yet, and that's not really something that we use a lot of. It's kind of specific to pesticide poisoning. So we don't worry about that.
You shouldn't worry about atropine. Here's the next one. You tell me what is going on with this patient. They have a toxicity.
What was it? Do they have a toxicity? Well, what kind? Anticholinergic.
Anticholinergic because we've got deoxybutylin. and the Benadryl. So those sent this poor little lady into an anticholinergic crisis.
So those medications are not supposed to be taken? Alright, those are two. Little old ladies and men don't really do well a lot of times with Benadryl.
Especially at way older years because it has like, it will make you sleepy and drowsy. They have more pronounced side effects because their bodies aren't organized as efficiently as a younger body. So it doesn't clear out as fast. So it's not a great medication for somebody who has a high risk of diabetes. I mean, I took Benadryl like a couple weeks ago just to go to sleep.
It's like I felt flubbed up the entire next day. So I'm early mid-ish 50s and if it's messing with me like that, then imagine what to do to a little 80 year old. Okay, so treatment.
It's kind of a little trick question. What's the first thing that we are going to do as nurses when this situation is brought to us? Run some fluids through it so it washes it out. Okay, so fluids.
Even before the fluids. That's what we're going to do. What would we expect to see on the vitals? So anticholinergic toxicity.
It's called heart rate. We have high blood pressure. We can see increased high blood pressure.
So here's the pulse rate. How are we fixing this? Given the antagonist, like the opposite of it, to counteract it, so cholinergic.
How do you say it? What kind of education are you doing? What side effects they could experience after getting this.
What else? Tell them the time. Why wouldn't you give them beta?
Oh, um, the, well we've got a, uh, we could to slow the heart rate, but for the most part, this one would be kind of stop the medicines and let them work out the system. And then say, "Nana, I know somebody's told you not to take that Benadryl." Why did you give me an albinadryl? Oh good, okay good answer. Very good answer for this class. Okay so we've talked about the fire and flight.
We've talked about all of these. The monists. So albuterol, airway.
Airway, beta-2. The beta agonists. One for the heart, two for the lungs. Clonidine, CNS. And clonidine we'll probably talk more about in the high blood pressure.
And dopamine, we're not worried about that right now. Now, for high blood pressure, I want you to tell me how if Prezosin, we know that it's an Alpha-1 blocker, you tell me where it's working at in the body. It's going to cause arterial dilation or constriction?
Dilation. Dilation. That's what we want to see.
because we'll talk about preloading more next week, but when you open up those veins, or arteries, I'm sorry, when you open up the arteries, it decreases the blood pressure. Atenolol, a beta-1 blocker, where is it working? The heart.
The heart. So, what effect is it having on the heart that you should see in your vital sign check? Slower heart rate. Slower heart rate. Now, propranolol, Beta 1 and beta 2. So it's your...
It affects both heart and lungs. We've got heart and lungs one up here. So this is one of the non-specific that if it hits the lungs, it can trigger an asthma attack. Not supporting you, Ricky, but it's like... Now we know how to off you, if need be.
So we're going to be off. So here. When somebody overdoses on a cholinergic drug, are you going to see dumbbells or Wait, you said dumbbells?
Are we going to see dumbbells or the mat as a hat? Dumbbells. Anaphylaxis. What are you going to shoot them up with? Epinephrine.
Why not more epinephrine? Because it doesn't activate the beta-2. Doesn't activate the beta-2. Then, propranolol.
Propranolol is going to do what to an asthmatic? Constrict. Drug class?
used for an overactive plant, sir? Cholinergic or anticholinergic? Cholinergic.
Anticholinergic. I'm just going to stop answering. Anticholinergic.
Is it any clearer now that it started? I'm going to go to you, Jesse. I'll put it like this.
It was clear creek trout water. Now it's mud water for carp. All right.
We'll flip that around. All right. As long as you remember the basics. What happens when this is activated versus what happens when...
I have time to go get my food now.